El uso Medicinal del Cannabis

La planta de cannabis se utilizó por miles de años en distintas culturas alrededor del mundo para distintos fines, entre ellos, la medicina. La planta posee distintos principios activos, denominados Cannabinoides. Estos Cannabinoides, en un número de más de 60, tienen distintas funciones, algunas descubiertas, y en su mayoría sin tener en claro aún cual es propósito. Estos Cannabinoides, por estar dentro de la planta se denominan Fitocannabinoides.

El cuerpo humano posee, en la superficie de muchos tipos de células de nuestro organismo, sitios específicos donde se acoplan estos  principios activos de la planta, los fitocannabinoides. Los más comunes, y de cuales se tiene mayor información son el THC, el CBD, CBG, CBN y algunos más. Los receptores de estos cannabinoides son denominados CB1 y CB2, encontrándose distribuidos por todo el cuerpo.El cuerpo humano también produce moléculas similares a las de la planta de cannabis, llamados endocannabinoides (endo=adentro). 

Los cannabinoides tienen muchas propiedades medicinales, y esto permite que algunas dolencias y patologías puedan ser tratadas con cannabis, tales como cáncer, epilepsia, glaucoma, esclerosis múltiple, fibromialgia, dolor crónico, etc.

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cannabinoids and epilepsy JUNIO 2018

Cannabinoids and epilepsy

 

1. Epilepsy Behav.

Proceedings of the Epilepsy Foundation's 2017 Cannabinoids in Epilepsy Therapy
Workshop.

Huizenga MN(1), Fureman BE(2), Soltesz I(3), Stella N(4).

Author information: 
(1)Department of Pharmacology and Physiology, Georgetown University, Washington, 
DC, United States. Electronic address: Esta dirección de correo electrónico está siendo protegida contra los robots de spam. Necesita tener JavaScript habilitado para poder verlo..
(2)Research and New Therapies, Epilepsy Foundation of America, Landover, MD,
United States.
(3)Department of Neurosurgery, Stanford Neurosciences Institute, Stanford
University, Stanford, CA, United States.
(4)Department of Pharmacology, University of Washington, Seattle, WA, United
States; Department of Psychiatry and Behavioral Sciences, University of
Washington, Seattle, WA, United States.


2. Int J Ment Health Addict. 2018;16(3):642-654. doi: 10.1007/s11469-017-9813-4.
Epub 2017 Sep 15.

Pregabalin Misuse and Abuse in Jordan: a Qualitative Study of User Experiences.

Al-Husseini A(1), Wazaify M(1), Van Hout MC(2).

Author information: 
(1)1Department of Biopharmaceutics and Clinical Pharmacy, School of Pharmacy, The
University of Jordan (UJ), Amman, Jordan.
(2)Public Health Institute, Liverpool John Moore's University, Liverpool, UK.

Pregabalin is currently approved for the treatment of epilepsy, generalized
anxiety disorder, neuropathic pain, and fibromyalgia. A qualitative study was
undertaken in Jordan, where concerns have been raised about its unprescribed
availability in community pharmacies and thereby its abuse. Semi-structured
interviews were conducted with all patients with a history of pregabalin use in
two Jordanian addiction treatment centers. All were male patients aged
21-30 years (n = 11). The majority was poly-drug abusers and had a previous
history of substance abuse (tramadol, Captagon, synthetic cannabinoids, and
marijuana). Six key themes emerged from a content textual analysis which centered
on pregabalin and other drugs; the pregabalin effect; poly-pharming and
pregabalin intoxication; trajectories, patterns, and routes of administration;
dependence and withdrawal; and sourcing of pregabalin. The study underscores the 
need for continued pharmacovigilance to manage and address suspected abuse, along
with community pharmacist and patient education regarding abuse liability and
related harms.


Conflict of interest statement: Compliance with Ethical StandardsEthical approval
was granted by the IRB at the Ministry of Health. The authors declare that they
have no conflict of interest.


3. Curr Treat Options Neurol.

Therapeutic Symptomatic Strategies in the Parasomnias.

Manni R(1), Toscano G(2), Terzaghi M(2).

Author information: 
(1)Sleep Medicine and Epilepsy Unit, IRCCS Mondino Foundation, Via Mondino,
27100, Pavia, Italy. Esta dirección de correo electrónico está siendo protegida contra los robots de spam. Necesita tener JavaScript habilitado para poder verlo..
(2)Sleep Medicine and Epilepsy Unit, IRCCS Mondino Foundation, Via Mondino,
27100, Pavia, Italy.

PURPOSE OF REVIEW: The purpose of this review was to discuss the currently
available pharmacologic and non-pharmacologic treatment options for parasomnias.
RECENT FINDINGS: Recent pathophysiological findings about sleep structure in
parasomnias helped understanding several drug mechanisms of action.
Serotoninergic theory accounts for the effect of serotoninergic drugs. Study
about spectral analysis of sleep showed the effect of clonazepam on spectral
bands. Cannabinoids proved to be effective in some of parasomnias, as in many
other neurological disorders. A series of therapeutic strategies were analyzed
and compared. Benzodiazepines, antidepressant drugs, and L-5-hydroxytryptophan
may be beneficial in DOA. SSRI and topiramate are effective in SRED. RBD responds
to clonazepam, melatonin, and to a lesser extent to dopaminergic and
anticholinergic agents. Prazosin and cannabinoids are effective in nightmare
disorder. Sleep paralysis may respond to antidepressant agents. Tricyclic
antidepressant may be effective in sleep-related hallucinations and exploding
head syndrome. Sleep enuresis may be successfully treated with desmopressin,
anticholinergic drugs, and imipramine.


4. Epilepsy Res.

Neuronal nitric oxide synthase is involved in CB/TRPV1 signalling: Focus on
control of hippocampal hyperexcitability.

Carletti F(1), Gambino G(2), Rizzo V(3), Ferraro G(4), Sardo P(5).

Author information: 
(1)Department of "Biomedicina Sperimentale e Neuroscienze Cliniche" (Bio.Ne.C.), 
"Sezione di Fisiologia umana G. Pagano", University of Palermo, Corso Tukory,
129-90134 Palermo, Italy. Electronic address: Esta dirección de correo electrónico está siendo protegida contra los robots de spam. Necesita tener JavaScript habilitado para poder verlo..
(2)Department of "Biomedicina Sperimentale e Neuroscienze Cliniche" (Bio.Ne.C.), 
"Sezione di Fisiologia umana G. Pagano", University of Palermo, Corso Tukory,
129-90134 Palermo, Italy. Electronic address: Esta dirección de correo electrónico está siendo protegida contra los robots de spam. Necesita tener JavaScript habilitado para poder verlo..
(3)Department of "Biomedicina Sperimentale e Neuroscienze Cliniche" (Bio.Ne.C.), 
"Sezione di Fisiologia umana G. Pagano", University of Palermo, Corso Tukory,
129-90134 Palermo, Italy. Electronic address: Esta dirección de correo electrónico está siendo protegida contra los robots de spam. Necesita tener JavaScript habilitado para poder verlo..
(4)Department of "Biomedicina Sperimentale e Neuroscienze Cliniche" (Bio.Ne.C.), 
"Sezione di Fisiologia umana G. Pagano", University of Palermo, Corso Tukory,
129-90134 Palermo, Italy. Electronic address: Esta dirección de correo electrónico está siendo protegida contra los robots de spam. Necesita tener JavaScript habilitado para poder verlo..
(5)Department of "Biomedicina Sperimentale e Neuroscienze Cliniche" (Bio.Ne.C.), 
"Sezione di Fisiologia umana G. Pagano", University of Palermo, Corso Tukory,
129-90134 Palermo, Italy. Electronic address: Esta dirección de correo electrónico está siendo protegida contra los robots de spam. Necesita tener JavaScript habilitado para poder verlo..

Cannabinoids (CB), transient receptors potential vanilloid type 1 (TRPV1) and
nitric oxide (NO) were found to be interlinked in regulating some neuronal
functions such as membrane excitability and synaptic transmission. TRPV1 play a
fundamental role since it represents a synaptic target for CB that triggers
several downstream cellular pathways. In this regard, recent evidence report that
TRPV1 could influence NO production by modulating neuronal NO synthase (nNOS)
activity. In the present research, we pointed to manipulate nNOS function to
assess its role on TRPV1 signalling in hyperexcitability conditions elicited in
the dentate gyrus of hippocampal formation. The activation of TRPV1 receptors is 
achieved by administering capsaicin (CAP), the main TRPV1 agonist exerting a
widely reported proepileptic effects. In order to focus on nNOS activity, we used
7-nitroindazole (7NI), nNOS inhibitor, or L-Arginine (ARG), NO precursor, before 
CAP. Then, the effects of each of these co-administration protocols were tested
in presence of WIN 55,212, a CB agonist. The study was conducted in rats using an
electrically-induced acute model of temporal lobe hyperexcitability, the Maximal 
Dentate Activation (MDA), considering different indicators of paroxysmal activity
such as: percentage of responses to electrical stimulation, MDA discharge
parameters and threshold current intensity for MDA. Data showed that the
excitatory effects of CAP were reduced by 7NI and enhanced by ARG pretreatments, 
respectively. In addition, the co-treatment with WIN counteracted CAP effect,
substantially resulting in an inhibitory effect. Finally, the CAP-WIN functional 
interaction appeared to be modulated by interfering with NO signalling since 7NI 
increased the inhibitory effect induced by the co-treatment with CAP and WIN,
whereas ARG reduced it. These findings suggest that nNOS function could be
involved in the CB/TRPV1 signalling and shed light on a new putative
cannabinoid-related control of neuronal hyperexcitability in the hippocampus.

Copyright © 2017 Elsevier B.V. All rights reserved.



5. Proc Natl Acad Sci U S A.

Cannabidiol attenuates seizures and social deficits in a mouse model of Dravet
syndrome.

Kaplan JS(1), Stella N(1)(2), Catterall WA(3), Westenbroek RE(1).

Author information: 
(1)Department of Pharmacology, University of Washington, Seattle, WA 98195.
(2)Department of Psychiatry and Behavioral Sciences, University of Washington,
Seattle, WA 98195.
(3)Department of Pharmacology, University of Washington, Seattle, WA 98195;
Esta dirección de correo electrónico está siendo protegida contra los robots de spam. Necesita tener JavaScript habilitado para poder verlo..

Worldwide medicinal use of cannabis is rapidly escalating, despite limited
evidence of its efficacy from preclinical and clinical studies. Here we show that
cannabidiol (CBD) effectively reduced seizures and autistic-like social deficits 
in a well-validated mouse genetic model of Dravet syndrome (DS), a severe
childhood epilepsy disorder caused by loss-of-function mutations in the brain
voltage-gated sodium channel NaV1.1. The duration and severity of thermally
induced seizures and the frequency of spontaneous seizures were substantially
decreased. Treatment with lower doses of CBD also improved autistic-like social
interaction deficits in DS mice. Phenotypic rescue was associated with
restoration of the excitability of inhibitory interneurons in the hippocampal
dentate gyrus, an important area for seizure propagation. Reduced excitability of
dentate granule neurons in response to strong depolarizing stimuli was also
observed. The beneficial effects of CBD on inhibitory neurotransmission were
mimicked and occluded by an antagonist of GPR55, suggesting that therapeutic
effects of CBD are mediated through this lipid-activated G protein-coupled
receptor. Our results provide critical preclinical evidence supporting treatment 
of epilepsy and autistic-like behaviors linked to DS with CBD. We also introduce 
antagonism of GPR55 as a potential therapeutic approach by illustrating its
beneficial effects in DS mice. Our study provides essential preclinical evidence 
needed to build a sound scientific basis for increased medicinal use of CBD.


Conflict of interest statement: The authors declare no conflict of interest.